Regulatory effect of interleukin-4 (IL-4) on the expression and function of lymphocyte adhesion receptors involved in IL-2-induced cell aggregation

F A Vyth-Dreese, Y Van Kooyk, T A Dellemijn, C J Melief, C G Figdor

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Human recombinant interleukin-4 (rIL-4) was studied for its capacity to inhibit rIL-2-induced lymphoid cell aggregation. In contrast to rIL-2, rIL-4 was unable to induce cluster formation by itself. However, when added simultaneously with rIL-2 to cultures of freshly isolated peripheral blood lymphocytes (PBL), rIL-4 inhibited cell aggregation in a dose-dependent way. In contrast, PBL, preactivated by a 4-day culture in the presence of 500 U/ml rIL-2, were not inhibited in their adhesive capacity by rIL-4. Inhibition of cell aggregation was most prominent at 24 hr and virtually lost after 72 hr of culture. Phenotypical analysis revealed that rIL-4, with similar kinetics, decreased the rIL-2-mediated up-regulation of the CD2, CD54 and CD49e adhesion molecules. In addition, it was observed that up-regulation of the activation epitope on CD11a recognized by the mAb NKI-L16, was prevented. During 24hr of culture rIL-4 itself did not alter the expression of these antigens. Blocking experiments with mAb directed against adhesion structures did not reveal a direct role for CD49e, but obviously demonstrated involvement of CD11a/CD18-CD54 and CD2-CD58 interactions in the rIL-2-induced adhesion. Therefore, rIL-4 appears to inhibit the early phase of rIL-2-induced aggregation by preventing the up-regulation of CD54 and CD2 antigens and by inhibiting the generation of the activated state of the CD11a/CD18 receptor.

Original languageEnglish
Pages (from-to)244-51
Number of pages8
Issue number2
Publication statusPublished - Feb 1993


  • Cell Adhesion Molecules/analysis
  • Cell Aggregation/drug effects
  • Cells, Cultured
  • Humans
  • Interleukin-2/antagonists & inhibitors
  • Interleukin-4/immunology
  • Kinetics
  • Receptors, Leukocyte-Adhesion/analysis
  • Recombinant Proteins/immunology

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